Celiac disease is an autoimmune disorder in which eating gluten proteins damages the villi of the small intestine causing food malabsorbion. It was described around the first part of the second century A.D. by Aretaeus of Cappadocia as a state in which the food is not broken down in the stomach but passes on undigested and is not absorbed. He called such patients “koiliakos,” after the Greek word “koelia,” meaning the abdomen.
In the early nineteenth century Dr. Mathew Baillie, probably unaware of Areteus’ description, wrote about a chronic diarrheal disorder of adults causing malnutrition and a gas-distended abdomen. He even suggested dietetic treatment, in that some of his patients benefited from living almost entirely on rice. His publication remained largely unnoticed and it was for Dr. Samuel Gee, physician and pediatrician at the Hospital for Sick Children at Great Ormond Street, to bring the disease to wider attention.
In 1888 Dr. Gee described celiac disease using the name given it by Areteus. He noted it occurred in children as well as in adults. Diarrhea was the chief manifestation, with bulky, pale, frothy, and ill smelling stools. There was also bloating, gas, abdominal pain, constipation, vomiting and often weight loss. Gee felt that cure would have to be by diet, that “the allowance of farinaceous food must be small,” and also described “a child who was fed upon a quart of the best Dutch mussels daily, throve wonderfully, but relapsed when the season for mussels was over.”
Later it became clear that celiac disease could occur without diarrhea, that breastfeeding was protective, and that the disease was more common in certain families and particularly in twins. There were new attempts to treat the disease by diet, such as the 1920 banana diet of Dr. Sidney Haas, which was successful in some patients and led him to the erroneous conclusion that celiac disease was caused by carbohydrates. But during World War II, Dr. Willem Dicke, a Dutch pediatrician, noticed that children with celiac disease improved when there were bread shortages but became worse after Allied planes dropped bread into the Netherlands. Working with others, he later produced a series of seminal papers, documenting for the first time the role that gluten from wheat and rye plays in celiac disease.
Many advances have occurred in subsequent decades. It became increasingly clear that celiac disease could be associated with a variety of other conditions. It was also apparent that clinical patterns of presentation were changing and that celiac disease was less of an intestinal disorder and causing more extra-intestinal symptoms and signs. In the late 1980’s a new apparatus made it possible to biopsy the distal duodenum showing atrophy of the villi of the intestinal mucosa. After 1990 celiac disease became increasingly accepted as an autoimmune condition of which the trigger (gluten) and the autoantigen (tissue transglutaminase) were known. Blood tests are now available to help with the diagnosis; the genetics of the disease are being increasingly understood; and new forms of treatment are being explored. But in the meanwhile a lifetime of living with a gluten-free diet remains by no means an easy task, as expounded in the article in this journal, “Not just a fad diet” by Jessica A. Nessat.
Read also: “Samuel Gee, Aretaeus, and the Coeliac Affection”, BMJ, 6 April 1974
GEORGE DUNEA, MD, Editor-in-Chief